Date: Tuesday, October 23, 2018
Session Title: Vasculitis Poster III: Immunosuppressive Therapy in Giant Cell Arteritis and Polymyalgia Rheumatica
Session Type: ACR Poster Session C
Session Time: 9:00AM-11:00AM
Background/Purpose: The effects of metabolic syndrome on vasculature are complex, and studies exploring the role of metabolic syndrome (including diabetes mellitus, obesity, hypertension, and hyperlipidemia) in the development and progression of giant cell arteritis (GCA) have been inconclusive. The objective of this retrospective study was to investigate how preexisting metabolic syndrome disorders impact the disease course, and if those with one or more disorders would require higher total cumulative steroid dose to achieve remission.
Methods: We identified GCA patients based on electronic medical record review using appropriate ICD-10 diagnosis codes. 51% of patients met ACR criteria for GCA. Selection criteria included time frame of 2008 – 2018, and actively being followed at our rheumatology clinics. We collected demographic, clinical, laboratory, imaging and histopathologic data for patients at the time of diagnosis through chart review. We used descriptive statistics for patient characteristics, and used regression analysis to investigate potential associations between metabolic syndrome disorders and total cumulative steroid treatment. Stepwise regression was used to determine the optimal regression model. We evaluated for potential confounding factors including age, gender, race and methotrexate (MTX) use.
Results: Our study population (n =35) was predominantly Caucasian (67%) and female (74%) with mean age at diagnosis of 62.4 ± 12.8 years. Metabolic syndrome was prevalent at or prior to the time of diagnosis in our group: 60% had hypertension, 23% had diabetes, 43% had hyperlipidemia and 43% were obese. Only two patients did not have any metabolic syndrome disorders. All patients received prednisone since their diagnosis, and 40% received MTX during their disease course. The mean total prednisone dose was 6780 ± 6457 mg. Regression analysis of individual metabolic disorders showed only significant association between hypertension and prednisone dosage, where on average, those with hypertension received 5986 mg less total prednisone (t = -2.249, p = 0.033). This result was not altered when accounting for age of onset, gender and race (t= -2.180, p = 0.040). However, when accounting for MTX use in subgroup analysis, the association between hypertension and total prednisone was no longer significant (t= -1.380, p = 0.217 with MTX; and t= -1.198, p = 0.256 without MTX). Stepwise regression of hypertension, age, gender, race and MTX use yielded a model including only hypertension and MTX. Stepwise regression including all metabolic syndrome diseases and potential confounders yielded a model including diabetes, obesity, hyperlipidemia, hypertension and MTX, where hypertension was the only variable significantly associated with prednisone dose (t= -2.550, p = 0.021).
Conclusion: Although a small cohort, our study population was similar in distribution when compared to larger cohorts studied previously. Contrary to our hypothesis, there were no metabolic disorders that were associated with significantly higher doses of cumulative prednisone dose. Further studies with larger study populations are needed to elucidate the complex interactions between metabolic syndrome and GCA.
To cite this abstract in AMA style:Guo W, Jandarov R, Gulati G. The Effect of Metabolic Syndrome on Giant Cell Arteritis Treatment [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 9). https://acrabstracts.org/abstract/the-effect-of-metabolic-syndrome-on-giant-cell-arteritis-treatment/. Accessed March 21, 2023.
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